Cardiovascular Disease Study Plan: Hypertension, Atherosclerosis, Coronary Artery Disease, | Exams Nursing | Docsity (2024)

Download Cardiovascular Disease Study Plan: Hypertension, Atherosclerosis, Coronary Artery Disease, and more Exams Nursing in PDF only on Docsity! NUR-3032 CARDIOVASCULAR DISEASE STUDY PLAN WITH VERIFIED SOLUTIONS Hypertension (6 questions): 1) Describe the neural mechanisms and humoral mechanisms that contribute to blood pressure regulation. How are the kidneys involved in the long-term regulation of blood pressure? Both control imbalance of b/p. Neural has Baroreceptors that respond to stretch in vessels. Humoral have the RAAS system and AHD effect. Both influenced by sympathetic and parasympathetic system. The kidneys will regulate B/P long term by retaining or secreting additional fluid. 2) Compare and contrast Primary (Essential) and Secondary Hypertension. Primary is of an unknown cause only by risk factors such as race (AA) and age. Secondary are results from other disorders such as lifestyle or obesity. 3) List 3 modifiable and 3 non-modifiable risk factors for Primary (essential) Hypertension. Modifiable 1. Lifestyle 2. alcohol 3. Obesity Non 1. Race 2. Age 3. Family history 4) What is considered a normal blood pressure? What is considered Prehypertensive? What is considered Stage I hypertension? What is considered stage 2 hypertension? How should blood pressure be measured and when should hypertension be diagnosed? Normal 120/80. Prehypertensive is 120-129 and <80 Stage I 130-139 OR 80-89 Stage 2 >140 OR greater or equal to>90A 5) Why is Primary (essential) hypertension considered a silent disorder? Some pt are asymptomatic, they experience headaches or eye pressure 6) List target-organ damage disorders associated with hypertension (i.e., diseases associated with the long-term effects of hypertension) ❖ Heart o LVH • Endothelial Damage (hom*ocysteine) 3) Compare and contrast the atherosclerotic lesions: fixed/stable plaque and unstable/vulnerable plaque. Fixed stable plaque form and stay in one area. Unstable plaque is a partial blockage and can rupture causing platelet aggregation. Can lead to thrombus. Or full blockage 4) What is Coronary Artery Disease? Describe the difference between acute coronary syndrome and chronic ischemic heart disease/ Heart disease with decreased coronary blood flow. Due to atherosclerosis. ACS-is plaque rupture, unstable angina and MI, ischemia leading to infarct. CIHD- recurrent MI or stable angina from vasospasm or atherosclerosis, narrowing of vessels. 5) Compare stable and unstable angina. Stable is obstructed blood flow by increased activity and relieved at rest or with nitroglycerin. 6) Compare the Acute Coronary Syndromes: Unstable Angina (UA), Non-ST Segment Elevated Myocardial Infraction (NSTEMI), and ST-Segment Elevated Myocardial Infarction (STEMI). • UA o Pathophysiology- unstable/vulnerable plaque that can rupture leading to thrombus formation. Can progress to an NSTEMI o Clinical Manifestations-pain at rest o Laboratory & Diagnostic Testing – ECG neg biomarkers • NSTEMI o Pathophysiology- The pathophysiology of UA/NSTEMI can be divided into five phases: o 1. The development of the unstable plaque that ruptures or plaque erosion with superimposed nonocclusive thrombosis o 2. An obstruction such as spasm, constriction, dysfunction, or adrenergic stimuli o 3. Severe narrowing of the coronary lumen o 4. Inflammation o 5. Any physiologic state causing ischemia related to decreased oxygen supply such as fever or hypotension o Clinical Manifestations: elevation of cardiac markers • The pain associated with UA/NSTEMI has a persistent and severe course and is characterized by at least one of three features: o 1. It occurs at rest (or with minimal exertion), usually lasting more than 20 minutes (if not interrupted by nitroglycerin). surrounding, noninfarcted area becomes thicker as it undergoes adaptive hypertrophy, so it can take over the work of the muscle in the infarcted zone. o Clinical Manifestations • The onset of STEMI usually is abrupt, with pain as the significant symptom. The pain typically is severe and crushing, often described as being constricting, suffocating, or like “something sitting on my chest.” It usually is substernal, radiating to the left arm, neck, or jaw, although it may be experienced in other areas of the chest. Unlike that of angina, the pain associated with STEMI is more prolonged and not relieved by rest or nitroglycerin, and narcotics frequently are required. Some persons may not describe it as “pain” but as “discomfort.” Women often experience atypical ischemic-type chest discomfort, whereas the elderly may complain of shortness of breath more frequently than chest pain. • Gastrointestinal complaints are common with STEMI. There may be a sensation of epigastric distress; nausea and vomiting may occur. These symptoms are thought to be related to the severity of the pain and vagal stimulation. The epigastric distress may be mistaken for indigestion, and the person may seek relief with antacids or other home remedies, which only delays getting medical attention. Complaints of fatigue and weakness, especially of the arms and legs, are common. Pain and sympathetic stimulation combine to give rise to tachycardia, anxiety, restlessness, and feelings of impending doom. A productive cough may be present with frothy, pink sputum. The skin often is pale, cool, and moist. Impairment of myocardial function may lead to hypotension and shock. • Sudden death from STEMI is death that occurs within 1 hour of symptom onset • o Laboratory & Diagnostic Testing: elevation of cardiac markers Deep Vein Thrombosis (DVT) (4 questions): 1) Review each of the following risk factors associated with venous thrombosis, including causes and pathophysiology: • Venous Stasis o Causes/Risk Factors o Pathophysiology Stasis of blood occurs with immobility of an extremity or the entire body. Bed rest and immobilization are associated with decreased blood flow, venous pooling in the lower extremities, and increased risk of DVT. People who are immobilized by a hip fracture, joint replacement, or spinal cord injury are particularly vulnerable to DVT. The risk of DVT is increased in situations of impaired cardiac function. This may account for the relatively high incidence in people with acute myocardial infarction and congestive heart failure. Older adults are more susceptible than younger people, probably because disorders that produce venous stasis occur more frequently in older adults. Long airplane travel poses a Risk factors for venous thrombosis include bed rest, immobility, spinal cord injury, acute myocardial infarction, congestive heart failure, shock, and venous obstruction. The Virchow triad illustrates three key factors leading to thrombus formation (see Fig. 26.19). • 2) What are the consequences of an untreated an untreated DVT? (hint: think emboli) DVT can lead to pulmonary embolism 3) How is a DVT diagnosed? Diagnostic tests that may be useful include venography, ultrasonography, and plasma d-dimer assessment. Heart Failure (7 questions): 1) Define the following terms: • Preload: reflects the volume or loading conditions of the ventricle at the end of diastole, just before the onset of systole. It is the volume of blood stretching the heart muscle at the end of diastole and is normally determined by the venous return to the heart. • Afterload: represents the force that the contracting heart muscle must generate to eject blood from the filled heart. The main components of afterload are the systemic (peripheral) vascular resistance and ventricular wall tension. • Myocardial Contractility/inotropy: refers to the contractile performance of the heart. It represents the ability of the contractile elements (actin and myosin filaments) of the heart muscle to interact and shorten against a load. Contractility increases cardiac output independent of preload and afterload. • Stroke Volume: how much blood it pumps with each beat • Ejection Fraction (what is a normal ejection fraction): Ejection fraction is the percentage of blood pumped out of the ventricles with each contraction. A normal ejection fraction is about 55% to 70%. distended and be visualized when sitting up or standing. • Left Ventricular Dysfunction/Left-Sided Heart Failure o auses/Risk Factors: hypertension and acute myocardial infarction. Stenosis or regurgitation of the aortic or mitral valve= pulmonary congestion= right sided heart failure o Pathophysiology: impairs the movement of blood from the low-pressure pulmonary circulation into the high-pressure arterial side of the systemic circulation. With impairment of left heart function, there is a decrease in cardiac output to the systemic circulation. Causes elevation in pulmonary venous pressure. o Clinical Manifestations: pulmonary edema often occurs at night Right heart failure Left heart failure | Congestion of peripheral tissues]| Decreased cardiac output} | Pulmonary congestion —edemaand ascites Gl tractcongestion Anorexia, Gl distress,weight lossSigns relatedto impaired liverfunctionActivityintoleranceand signs ofdecreasedtissueperfusion Impaired gas Pulmonaryexchange edemaOrthopneaCyanosisand signs ofhypoxiaCough with Paroxysmalfrothy sputum nocturnal dyspnea4) Describe the compensatory mechanisms for heart failure. Frank-Starling mechanism, activation of neurohumoral influences such as the sympathetic nervous system reflexes, the renin–angiotensin–aldosterone mechanism, cardiac NPs, locally produced vasoactive substances, and myocardial hypertrophy and remodeling 5) Describe the 4 classes of the New York Heart Association (NYHA) Functional Classification (hint: see Porth textbook, page 878) 1. Class I—People who have known heart disease without symptoms during ordinary activity 2. Class II—People who have heart disease who have slight limitations but not extreme fatigue, palpitations, dyspnea, or angina pain during regular activity 3. Class III—People with heart disease who are comfortable at rest but ordinary activity does result in fatigue, palpitations, dyspnea, and angina pain 4. Class IV—People who have marked progressive cardiac disease and are not comfortable at rest or minimal activity